Copernicus revisited: amyloid beta in Alzheimer's disease

Citation
J. Joseph et al., Copernicus revisited: amyloid beta in Alzheimer's disease, NEUROBIOL A, 22(1), 2001, pp. 131-146
Citations number
189
Language
INGLESE
art.tipo
Editorial Material
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROBIOLOGY OF AGING
ISSN journal
0197-4580 → ACNP
Volume
22
Issue
1
Year of publication
2001
Pages
131 - 146
Database
ISI
SICI code
0197-4580(200101/02)22:1<131:CRABIA>2.0.ZU;2-A
Abstract
The beta-amyloid hypothesis of Alzheimer's Disease (AD) has dominated the t hinking and research in this area for over a decade and a half. While there has been a great deal of effort in attempting to prove its centrality in t his: devastating disease, and while an enormous amount has been learned abo ut its properties (e.g.. putative toxicity, processing and signaling), A be ta has not proven to be both necessary and sufficient for the development, neurotoxicity, and cognitive deficits associated with this disease. Instead , the few treatments that are available have emerged from aging research an d are primarily directed toward modification of acetylcholine levels. Clear ly, it is time to rethink this position and to propose instead that future approaches should focus upon altering the age-related sensitivity of the ne uronal environment to insults involving such Factors as inflammation and ox idative stress. In other words "solve the problems of aging and by extensio n those of AD will also be reduced." This review is being submitted as a ra ther Lutherian attempt to "nail an alternative thesis" to the gate of the C hurch of the Holy Amyloid to open its doors to the idea that aging is the m ost pervasive element in this disease and A beta is merely one of the plane ts. (C) 2001 Elsevier Science Inc. All rights reserved.